This invention relates generally to systems and arrangements for inhibiting the development of pressure sores, and more particularly to methods and arrangements for stimulating electrically in the region of a pressure communication where development of pressure sores can reasonably be expected.
It is well known that many physically disabled persons experience skin ulcerations, or pressure sores, when the skin is subjected to external pressure. The probability of developing pressure sores increases with the time over which the external pressure is applied, particularly if the pressure is applied without relief. The pressure sores which result from such relentless pressure are known by a variety of names, including "decubitus ulcers," "pressure sores," "ischemic sores," "bed sores," etc. Such sores, which will generally be referred to herein as "pressure sores," are a particular problem for individuals who are dependent upon wheelchairs. Many such individuals lack sensation in the buttocks.
Pressure sores are formed as a consequence of a number of intrinsic and extrinsic factors, including the magnitude of applied tissue force, force direction (i.e., normal versus shear), duration of applied force, friction, tissue hygiene, circulatory health, nutritional health, and other factors promoting tissue ischemia. The degree and duration of applied tissue pressure is recognized as an important factor in the formation of pressure sores. Any continued pressure sufficient to obstruct blood circulation for more than a few hours will lead to tissue necrosis and the probable formation of an ulcer or pressure sore.
It is known that increased tissue pressure creates ischemia resulting in the development of ulcers in muscle, skin, and other connective tissue. The microscopic changes in animal muscle resulting from the application of pressure were found to consist of edema, loss of cross-striations and myofibrials, hyalinization of fibers, neutrophilic infiltration, and phagocytosis by neutrophilis and macrophages. Changes in tissue produced after the application of localized pressure have been demonstrated to be primarily the result of ischemia. Intense pressure can cause complete cessation of capillary circulation and also results in the formation of venous thrombosis. The presence of venous thrombi then interferes with the normal reactive hyperemic vasodilation after the pressure is removed, resulting in continued ischemia.
The primary cause of tissue death with ischemia is due to reduced oxygen delivery and metabolite removal. Mean capillary pressure does not appear to be the primary parameter in the development of ischemia at the capillary level. Tissue ischemia can result from both supra and sub-normal capillary pressure, depending upon the direction of the applied force. Duration of the applied force, as well as force magnitude, is a critical factor in the formation of pressure sores. Researchers have found an inverse time-pressure relationship for the formation of pressure sores in laboratory animals. When the applied pressure is high enough to interfere with tissue circulation and is applied for a sufficient length of time, skin breakdown results. Duration of external pressure can be a more important factor in producing tissue damage than pressure magnitude.
Distortion and the eventual occlusion of blood vessels are primary results of uniaxial forces. The body tissue is essentially incompressible, so that during simple uniaxial compression, lateral expansion must occur to the extent required to maintain constant volume. This tissue distortion tends to collapse blood vessels and promote ulcer formation. Hydrostatic loading, on the other hand, avoids tissue distortion, a major factor in blood vessel occlusion. Thus, tissue distortion which occurs as a result of external forces, is a main factor in the development of pressure sores. Such external forces may be measured as increased pressure at the interface between the skin and a surface.
Shearing forces are also a significant factor in the formation of pressure sores. Non-homogeneity of skin results in increased stress and strain at the interfaces between the skin, underlying fat, fascia, muscle, and bone, with externally applied shear forces. This can be of special significance at the interface of the skin and subcutaneous tissues as many of the blood vessels which supply the skin enter this interface at right angles to its boundary. Forces in the plane of the skin produce deformation and bending in the vessels, therefore leading to ischemia. This can result in larger areas of ischemia when dealing with shear forces as compared to normal forces.
Other factors, in addition to the magnitude and duration of the normal and shear forces, have been found to play important roles in the formation of pressure sores. Friction, for example, increases the susceptibility of skin ulceration at constant pressure. Pressures of 45 mm Hg were found to cause ulcer formation when frictional forces were present. However, a pressure of 290 mm Hg was required to produce ulcers in swine with no friction present. Using isotope clearance techniques, it has been concluded that friction increases the production of ulcers by mechanical damage of the skin and not by an ischemic mechanism.
Several other secondary factors are invloved in the formation of pressure sores. Poor circulation conditions, edema, and anemia are all contributing factors in the formation of decubitus ulcers due to their restriction of oxygen delivery and metabolic processes. Moisture in the form of perspiration, urine, or feces, greatly contributes to the risk of ulcer formation. Pressure sores could be prevented by relieving body compression and washing the body daily to remove urine and feces. Keeping the skin clean and adequately ventilated is necessary to reduce bacterial growth and help prevent pressure sores.
Skin temperature is another important factor in the formation of pressure sores. Cold temperatures can facilitate development by promoting tissue ischemia via vasoconstriction. Hot temperatures, locally or in the form of fever, are also known to contribute to tissue breakdown. High temperatures contribute to cellular metabolic deficiency by increasing the metabolic rate, and hence, the tissue demand for blood and oxygen. This increased demand can be extremely detrimental when the blood supply is already compromised because of compression. High temperatures also increase the rate of sweat formation which has already been noted as a factor in the formation of pressure sores.
Two forms of pressure sores can be distinguished. The first is superficial and begins in the skin surface with maceration of devitalized skin. If permitted to progress, an infected shallow ulcer may be formed which is often painful for sensate individuals. The second type of pressure sore is the deep sore which arises in tissues overlying bony prominances and later extends to the surface. In this form, the progress of the tissue damage is from within to without and considerable necrosis of muscle, fascia, and subcutaneous tissue may have occurred even at a stage when the skin shows only erythema. Later, gangrenous lesions extend through the skin, and in some cases, down to underlying bone.
The financial costs for treating pressure sores are staggering. The average cost for hospitalized treatment of a pressure sore has been estimated at well over $15,000.00. Recently, cost of $20,000.00 to $30,000.00 per incident have been estimated. The annual price tag for medical care costs associated with pressure sores exceeds $2,000,000,000.00, and it is estimated that insurers allot 25% of anticipated spinal cord injury medical expenses for the treatment of pressure sores.
In addition to such financial costs, individuals afflicted with pressure sores also experience loss of work, reduced independence, inability to attend school, lowered self-esteem, particularly when forced to lay prone for periods of weeks or months, as well as other psychological burdens which are bourne by those afflicted and their families. Clearly, the problem is a devastating one, and there is a great need from both economic considerations and quality of life issues, for investigating new and more effective approaches to the problem. These problems, however, perhaps pale in the light of the fatality rate associated with pressure sores. The Veterans' Administration has estimated that 50% of all quadraplegic veterans and 30% of paraplegics will require hospitalization during their lifetime for pressure sore related problems. The Veterans' Administration also estimated that approximately 25% of these patients would die as a direct consequence of pressure sores.
In response to this urgent need, there is available in the prior art a large variety of mattresses, special beds, wheelchair cushions and other support systems. Most such systems are designed to reduce pressures or distribute them more evenly over the body. Although some of these devices have succeeded commercially, none seems to provide a universal solution to the problem of ulcer formation.
It is, therefore, an object of this invention to provide a simple and relatively inexpensive system for inhibiting the development of pressure sores.
It is also an object of this invention to provide a system which reduces the risks of pressure sores without restricting wheelchair mobility.
It is another object of this invention to provide a system for inhibiting the development of pressure sores, which can be used by sensate and insensate individuals.